Influenza A virus
subtype H3N2
Influenza A virus subtype H3N2 is a strain of influenza A virus that can infect humans, as well as pigs and birds. It is one of the three subtypes of influenza A virus that commonly cause seasonal flu outbreaks in humans, the other two being H1N1 and influenza B.
H3N2 influenza virus is known for its ability to mutate rapidly, which can make it difficult to develop effective vaccines against it. This strain of the flu can cause a range of symptoms, from mild to severe, and it can lead to complications such as pneumonia, bronchitis, and sinus infections.
The symptoms of H3N2 influenza are similar to those of other types of flu, including fever, cough, sore throat, body aches, fatigue, and sometimes vomiting and diarrhea. The virus is transmitted through respiratory droplets when an infected person coughs or sneezes.
- symptoms
- Types of virus
- Genome and structure
- Life cycle
- Antigenic
- Transmission
- Pathophysiology
- Immunology
- History
- Conclusion
Signs and symptoms
The time between openness to the infection and
advancement of side effects, called the hatching period, is 1-4 days, most
generally 1-2 days. Numerous diseases, nonetheless, are asymptomatic. The
beginning of side effects is unexpected, and introductory side effects are
predominately vague, including fever, chills, migraines, muscle torment or
hurting, a sensation of distress, loss of craving, absence of energy/weariness,
and disarray. These side effects are normally joined by respiratory side
effects like a dry hack, sore or dry throat, dry voice, and a stodgy or runny
nose. Hacking is the most widely recognized side effect. Gastrointestinal side
effects may likewise happen, including sickness, retching, loose bowels, and
gastroenteritis, particularly in kids. The standard flu side effects commonly
keep going for 2-8 days. A recent report proposes flu can make durable side
effects likewise lengthy Coronavirus.
Indicative contaminations are typically gentle and
restricted to the upper respiratory parcel, yet movement to pneumonia is
generally normal. Pneumonia might be brought about by the essential viral
contamination or by an optional bacterial disease. Essential pneumonia is
portrayed by fast movement of fever, hack, worked breathing, and low oxygen
levels that cause pale blue skin. Particularly normal among those have a
fundamental cardiovascular infection like rheumatic coronary illness. Optional
pneumonia ordinarily has a time of progress in side effects for 1-3 weeks
followed by repetitive fever, sputum creation, and liquid development in the
lungs, however can likewise happen only a couple of days after flu side effects
show up. About 33% of essential pneumonia cases are trailed by auxiliary
pneumonia, which is most often brought about by the microorganisms
Streptococcus pneumonia and Staphylococcus aureus.
Types of virus
Flu infections involve four species. Every one of the
four animal categories is the sole individual from its own class, and the four
flu genera contain four of the seven genera in the family Orthomyxoviridae.
They are:
- · Flu
A infection (IAV), class Alphainfluenzavirus
- · Flu
B infection (IBV), sort Betainfluenzavirus
- · Flu
C infection (ICV), sort Gammainfluenzavirus
- · Flu
D infection (IDV), sort Deltainfluenzavirus
IAV is answerable for most instances of serious
disease as well as occasional scourges and infrequent pandemics. It
contaminates individuals of any age however will in general excessively cause
extreme disease in the old, the exceptionally youthful, and the people who have
persistent medical problems. Birds are the essential repository of IAV,
particularly amphibian birds like ducks, geese, shorebirds, and gulls, however
the infection additionally courses among well evolved creatures, including
pigs, ponies, and marine vertebrates. IAV is ordered into subtypes in light of
the viral proteins haemagglutinin (H) and neuraminidase (N). Starting around
2019, 18 H subtypes and 11 N subtypes have been recognized. Most potential
mixes have been accounted for in birds, yet H17-18 and N10-11 have just been
viewed as in bats. Just H subtypes H1-3 and N subtypes N1-2 are known to have
coursed in people, the ongoing IAV subtypes available for use being H1N1 and
H3N2. IAVs can be characterized all the more explicitly to likewise incorporate
regular host species, geological beginning, year of detachment, and strain
number, like H1N1/A/duck/Alberta/35/76.
IBV fundamentally contaminates people yet has been
distinguished in seals, ponies, canines, and pigs. IBV doesn't have subtypes
like IAV yet has two antigenically unmistakable heredities, named the
B/Victoria/2/1987-like and B/Yamagata/16/1988-like ancestries, or just
(B/)Victoria(- like) and (B/)Yamagata(- like). The two ancestries are available
for use in people, lopsidedly influencing kids. IBVs add to occasional
pestilences close by IAVs however have never been related with a pandemic.
ICV, as IBV, is basically tracked down in people,
however it likewise has been recognized in pigs, wild canines, dromedary
camels, steers, and canines. ICV disease essentially influences kids and is
typically asymptomatic or has gentle cold-like side effects, however more
extreme side effects, for example, gastroenteritis and pneumonia can happen.
Dissimilar to IAV and IBV, ICV has not been a significant focal point of
examination relating to antiviral medications, immunizations, and different
measures against flu. ICV is subclassified into six hereditary/antigenic
genealogies.
IDV has been disconnected from pigs and dairy cattle,
the last option being the regular supply. Contamination has additionally been
seen in people, ponies, dromedary camels, and little ruminants like goats and
sheep. IDV is indirectly connected with ICV. While steers laborers have
sporadically tried positive to earlier IDV contamination, causing illness in
humans isn't known. ICV and IDV experience a more slow pace of antigenic
development than IAV and IBV. In view of this antigenic steadiness, moderately
barely any original heredities arise.
Genome and structure
Flu infections have a negative-sense, single-abandoned
RNA genome that is divided. The negative feeling of the genome implies it tends
to be utilized as a format to combine courier RNA (mRNA). IAV and IBV have
eight genome sections that encode 10 significant proteins. ICV and IDV have
seven genome sections that encode nine significant proteins. Three sections
encode three subunits of a RNA-subordinate RNA polymerase (RdRp) complex: PB1,
a transcriptase, PB2, which perceives 5' covers, and Dad (P3 for ICV and IDV),
an endonuclease. The grid protein (M1) and film protein (M2) share a section,
as do the non-underlying protein (NS1) and the atomic commodity protein (NEP).
For IAV and IBV, hemagglutinin (HA) and neuraminidase (NA) are encoded on one
section each, though ICV and IDV encode a hemagglutinin-esterase combination
(HEF) protein on one fragment that blends the elements of HA and NA. The last genome
fragment encodes the viral nucleoprotein (NP). Flu infections likewise encode
different embellishment proteins, for example, PB1-F2 and Dad X, that are
communicated through elective open understanding edges and which are
significant in have guard concealment, harmfulness, and pathogenicity.
The infection molecule, called a virion, is
pleomorphic and changes between being filamentous, bacilliform, or round in
shape. Clinical disconnects will more often than not be pleomorphic, though
strains adjusted to research center development ordinarily produce round
virions. Filamentous virions are around 250 nanometers (nm) by 80 nm,
bacilliform 120-250 by 95 nm, and circular 120 nm in width. The virion
comprises of each fragment of the genome bound to nucleoproteins in discrete
ribonucleoprotein (RNP) buildings for each section, which are all encircled by
a lipid bilayer film called the viral envelope. There is a duplicate of the
RdRp, all subunits included, bound to each RNP. The envelope is built up
basically by grid proteins on the inside that encase the RNPs, and the envelope
contains HA and NA (or HEF) proteins broadening outward from the outside
surface of the envelope. HA and HEF proteins have a particular "head"
and "tail" structure. M2 proteins structure proton particle channels
through the viral envelope that are expected for viral section and exit. IBVs
contain a surface protein named NB that is secured in the envelope, however its
capability is obscure.
Life cycle
The life cycle of influenza virus is a complex process
that involves multiple stages, starting from the initial attachment of the
virus to the host cell and ending with the release of new virions from the
infected cell. Here is a brief overview of the influenza virus life cycle:
Attachment:
The attachment stage of the influenza virus life cycle is initiated by the
hemagglutinin (HA) protein on the surface of the virus. The HA protein binds to
sialic acid receptors on the surface of the host cell, which allows the virus
to attach to the host cell and initiate infection. The specificity of the HA
protein for certain sialic acid receptors determines which host cells the virus
can infect.
Entry: After the virus
attaches to the host cell, it is internalized into the cell through a process
called endocytosis. During endocytosis, the virus is engulfed by a portion of
the host cell membrane, which forms a vesicle called an endosome. The virus
then uses the acidic environment of the endosome to fuse its lipid envelope
with the endosomal membrane, releasing the viral genome into the cytoplasm of
the host cell.
Fusion: Once the virus
has entered the host cell cytoplasm, the viral RNA genome is released and
transported to the host cell nucleus. There, the viral RNA is transcribed into
messenger RNA (mRNA) by the host cell machinery, which is then translated into
viral proteins.
Replication:
The viral mRNA is translated into viral proteins, which are used to assemble
new virions. The viral genome consists of eight segments of RNA, which are
replicated and packaged into new virions in the host cell nucleus.
Assembly:
The viral proteins and RNA segments are assembled into new virions in the host
cell nucleus. The newly synthesized viral components are then transported to
the host cell membrane, where they are assembled into new virions.
Budding: Once the new
virions have been assembled at the host cell membrane, they bud off from the
membrane, acquiring a lipid envelope from the host cell membrane. This process
allows the virus to escape from the infected host cell and spread to new host
cells.
Release: The final stage
in the life cycle of the influenza virus is the release of the newly formed
virions into the extracellular space. The released virions can then infect new
host cells and continue the cycle of infection.
The life cycle of the influenza virus is a complex
process that involves multiple stages of attachment, entry, fusion,
replication, assembly, budding, and release. The virus uses its surface
proteins and lipid envelope to infect host cells and hijack the host cell
machinery to replicate and assemble new virions. Understanding the life cycle
of the influenza virus is important for developing effective treatments and
vaccines to prevent and control influenza infections.
Antigenic
Antigenic drift and antigenic shift are two ways that
influenza viruses evolve to evade host immunity and cause disease. These
mechanisms play a crucial role in the development of seasonal and pandemic
influenza outbreaks.
Antigenic drift is a gradual change in the surface
proteins of influenza viruses, hemagglutinin (HA) and neuraminidase (NA), which
results in the accumulation of small mutations in the viral genome over time.
These mutations alter the structure of the HA and NA proteins, causing the
virus to become less recognizable to host immune systems. As a result, antibodies
produced in response to previous infections or vaccinations may not be
effective in protecting against the drifted virus. Antigenic drift is
responsible for the annual variation in influenza strains and the need for
yearly updates to influenza vaccines.
Antigenic shift is a more dramatic change in the
surface proteins of influenza viruses that occurs when two different influenza
viruses infect the same host cell and exchange genetic material. This can
result in the creation of a new virus with a novel HA or NA protein that is not
recognized by the host immune system. Antigenic shift can lead to the emergence
of pandemic influenza strains, which can cause widespread illness and death.
The 1918, 1957, 1968, and 2009 influenza pandemics were all caused by antigenic
shift.
The influenza virus is particularly prone to antigenic
drift and shift because it is an RNA virus, which has a high mutation rate and
lacks proofreading mechanisms to correct errors during replication.
Additionally, the virus can infect multiple species, including birds, swine,
and humans, which provides opportunities for genetic exchange and antigenic
shift.
To monitor the evolution of influenza viruses, the
World Health Organization (WHO) and other public health organizations conduct
global surveillance of influenza strains, collecting data on their antigenic
characteristics and resistance to antiviral drugs. This information is used to
update influenza vaccines and to develop strategies for pandemic preparedness.
In summary, antigenic drift and antigenic shift are
mechanisms by which influenza viruses evolve to evade host immunity and cause
disease. Antigenic drift is a gradual change in the surface proteins of the
virus, while antigenic shift is a more dramatic change that results from the
exchange of genetic material between different viruses. These mechanisms
contribute to the ongoing evolution of influenza viruses and the need for
continued surveillance and development of effective vaccines and treatments.
Transmission
Influenza is a highly contagious respiratory illness
caused by the influenza virus. The virus spreads from person to person through
respiratory droplets generated when an infected person coughs, sneezes, or
talks. The transmission of influenza is facilitated by a combination of
factors, including the virus's ability to survive on surfaces and its ability
to mutate rapidly.
The primary mode of transmission of influenza is
through direct contact with respiratory droplets from infected individuals.
These droplets can be inhaled by individuals in close proximity to the infected
person, usually within 6 feet. The droplets can also land on surfaces and
objects, where they can survive for several hours, and infect individuals who
touch these contaminated surfaces and then touch their nose or mouth.
Influenza can also be transmitted through airborne
particles, particularly in enclosed spaces with poor ventilation. This is
particularly true for certain settings such as crowded schools, nursing homes,
and hospitals, where large numbers of people are in close contact with one
another. Airborne transmission occurs when an infected person expels small
particles that can remain suspended in the air and be inhaled by others.
Additionally, it is possible for influenza to be
transmitted through contact with infected animals, particularly birds and pigs.
This type of transmission is less common in humans but can occur in individuals
who have close contact with infected animals or who work in the poultry or
swine industry.
Influenza can be particularly dangerous for
individuals who are at high risk of complications, including young children,
older adults, pregnant women, and individuals with underlying health conditions
such as asthma, diabetes, and heart disease. To reduce the spread of influenza,
it is important to practice good respiratory hygiene, such as covering coughs
and sneezes, washing hands frequently, avoiding close contact with individuals
who are sick, and staying home when sick. Vaccination is also an effective way
to prevent influenza and reduce its transmission in the community.
Pathophysiology
Influenza is a viral infection that primarily affects
the respiratory system. The pathophysiology of influenza involves the
interaction between the virus and the host immune system, leading to a range of
symptoms and potential complications.
The influenza virus enters the body through the
respiratory tract, where it attaches to and infects the epithelial cells lining
the respiratory tract. The virus then replicates within these cells, leading to
destruction of the infected cells and the release of new virus particles that
can infect neighboring cells. This process can cause inflammation and damage to
the respiratory tract, leading to symptoms such as cough, sore throat, and
shortness of breath.
As the virus replicates, it also triggers an immune
response in the body. The immune response involves the activation of immune
cells such as T cells, B cells, and antibodies, which work to identify and
destroy the virus. The immune response can also lead to the release of
cytokines, small signaling molecules that help to coordinate the immune
response. However, in some cases, the immune response can become dysregulated,
leading to excessive cytokine release and a systemic inflammatory response.
This can result in more severe symptoms, such as fever, fatigue, and muscle
aches.
Influenza can also lead to a range of potential
complications, particularly in individuals who are at high risk. Complications
can include pneumonia, bronchitis, sinus infections, and ear infections, among
others. These complications can be caused by the direct effects of the virus on
the respiratory tract, as well as by secondary bacterial infections that can
occur as a result of the weakened immune system.
The pathophysiology of influenza involves the
interaction between the virus and the host immune system, leading to a range of
symptoms and potential complications. The virus replicates within the
respiratory tract, leading to destruction of infected cells and the release of
new virus particles. The immune response is activated to fight the virus, which
can result in cytokine release and systemic inflammation. Complications can
occur as a result of the direct effects of the virus on the respiratory tract
or from secondary bacterial infections.
Immunology
Influenza is an infectious disease caused by the
influenza virus, which primarily affects the respiratory system. The immunology
of influenza involves the interaction between the virus and the host immune
system, including the innate and adaptive immune responses.
Innate immune response:
The innate immune response is the first line of
defense against the influenza virus. It involves the activation of immune cells
such as dendritic cells, macrophages, and natural killer cells, which recognize
and respond to the virus. These cells produce cytokines, which help to
coordinate the immune response and recruit other immune cells to the site of
infection. The innate immune response is important in controlling the initial
stages of the infection and limiting the spread of the virus.
Adaptive immune response:
The adaptive immune response is a more specific
response that develops over time as the immune system learns to recognize and
respond to the influenza virus. It involves the activation of T cells and B
cells, which work together to eliminate the virus and provide long-term
protection against future infections.
T cells:
T cells are a type of immune cell that play a key role
in the adaptive immune response to influenza. They recognize and respond to
viral antigens, which are proteins on the surface of the virus. There are two
types of T cells that are important in the response to influenza: CD4+ T cells
and CD8+ T cells. CD4+ T cells help to activate other immune cells, such as B
cells and CD8+ T cells, and also help to coordinate the immune response. CD8+ T
cells are cytotoxic T cells that can directly kill infected cells.
B cells:
B cells are a type of immune cell that produce
antibodies, which are proteins that can recognize and bind to viral antigens.
Antibodies can neutralize the virus by preventing it from infecting host cells,
and they can also help to activate other immune cells, such as macrophages and
natural killer cells. B cells can also undergo somatic hypermutation, a process
that allows them to produce antibodies with higher affinity for the virus over
time.
Memory response:
The adaptive immune response to influenza also leads
to the development of memory cells, which are immune cells that can recognize
and respond to the virus more quickly and efficiently in the event of a future
infection. Memory cells can provide long-term protection against the virus,
which is the basis for influenza vaccination.
The immunology of influenza involves the interaction
between the virus and the host immune system, including the innate and adaptive
immune responses. The innate immune response provides the initial defence
against the virus, while the adaptive immune response involves the activation
of T cells and B cells, which work together to eliminate the virus and provide
long-term protection. The development of memory cells is the basis for
influenza vaccination, which is an effective way to prevent influenza and
reduce its spread in the community.
History
Influenza is a viral disease that has been known to
affect humans for centuries. The history of influenza is marked by several
pandemics and outbreaks that have caused significant morbidity and mortality
throughout the world.
The first recorded pandemic of influenza occurred in
1580, and subsequent pandemics have occurred approximately every 10-50 years
since then. The deadliest pandemic of the 20th century was the Spanish flu
pandemic of 1918-1919, which infected approximately 500 million people and
caused an estimated 50 million deaths worldwide. The virus responsible for the
Spanish flu was an H1N1 strain of influenza A.
Since then, there have been several other pandemics of
influenza, including the Asian flu pandemic of 1957-1958, the Hong Kong flu
pandemic of 1968-1969, and the most recent pandemic, the H1N1 pandemic of
2009-2010. The H1N1 pandemic was caused by a novel strain of influenza A virus
that emerged in Mexico in 2009, and it infected an estimated 1 billion people
worldwide, causing an estimated 284,000 deaths.
In addition to pandemics, there have been numerous
seasonal outbreaks of influenza throughout history. Influenza outbreaks occur
every year, typically during the winter months, and can cause significant
morbidity and mortality, particularly in vulnerable populations such as the
elderly, young children, and individuals with underlying medical conditions.
The history of influenza has been marked by
significant advances in our understanding of the virus and its transmission, as
well as the development of vaccines and antiviral medications to prevent and
treat the disease. Influenza vaccines are now widely available and recommended
for individuals of all ages, and antiviral medications can help to reduce the
severity of symptoms and prevent complications in individuals who are infected
with the virus.
Summary
Influenza is a viral disease that has affected humans
for centuries, with several pandemics and outbreaks occurring throughout
history. The most deadly pandemic was the Spanish flu pandemic of 1918-1919,
which caused an estimated 50 million deaths worldwide. Since then, there have
been several other pandemics and seasonal outbreaks of influenza. Advances in
our understanding of the virus and the development of vaccines and antiviral
medications have helped to reduce the impact of the disease, but influenza remains
a significant public health concern. Influenza vaccines are widely available
and recommended for individuals of all ages, and antiviral medications can help
to reduce the severity of symptoms and prevent complications in individuals who
are infected with the virus.